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Background: EMILIN2 is a platelet-associated elastin that regulates angiogenesis. It has recently been found to play an essential role in various tumors. Nevertheless, the mechanism of action of EMILIN2 in clear cell renal cell carcinoma (ccRCC) remains unclear.Methods: Samples from 33 cancers were obtained from UCSC Xena and The Cancer Genome Atlas (TCGA) database. The relationship between EMILIN2 expression and the clinicopathological characteristics and immune infiltration of ccRCC was investigated. Nonnegative matrix factorization (NMF) was used to classify ccRCC patients. A multigene risk prediction model of ccRCC was constructed using LASSO regression and multivariate regression analysis. A nomogram survival probability prediction map and calibration curve were constructed based on clinical information.Results: EMILIN2 is significantly overexpressed in ccRCC, a phenomenon that is associated with poor prognosis. Meanwhile, EMILIN2 expression is closely related to tumor immune infiltration in ccRCC. Patients with clear cell renal cell carcinoma were divided into two subtypes using NMF, with subtype 2 showed poor prognosis. Next, we established a risk score model for ccRCC based on the common differentially expressed genes (DEGs) between subtypes and groups based on EMILIN2 expression. The results indicated poor prognosis in the high-risk group in the training set and were confirmed in the validation set.Conclusion: Our findings suggest that EMILIN2 expression is closely associated with immune infiltration in ccRCC. EMILIN2 expression is negatively correlated with the prognosis of ccRCC patients. Here, we developed a tool that could predict the prognosis of ccRCC patients.

Immune checkpoint inhibitors (ICIs) including PD-1/PD-L1 antibodies, have demonstrated significant clinical benefits in the treatment of individuals with many types of cancer. However, as more and more patients use such therapies, the side effects of immune checkpoint inhibitors have also been discovered. These include accelerated tumor growth in some patients, creating new lesions, and even life-threatening ones. These side effects are known as hyperprogression disease (HPD), and different types of tumors have different HPD conditions after ICIs treatment. Therefore, understanding the pathogenesis of HPD and predicting its occurrence is critical for patients using ICIs therapy. Here, we will briefly review the current status of PD-1/PD-L1 antibody therapy, HPD occurrence in various types of tumors, and the underlying mechanism.

Reactive oxygen species (ROS), a class of reactive oxidants, play critical roles in signal transduction, cell metabolism, immune defense and other physiological processes. Abnormally excessive levels of ROS can cause diseases and thus, investigations into the relevant biology and medicine are significant. The behavior of ROS in inflammation has been rarely elucidated. In this work, two ROS fluorescent probes, FS-ROS1 and FS-ROS2 have been designed and synthesized. FS-ROS1 responds rapidly (~1 min) to ClO- and gradually (~ 30 min) to H2O2 with an increase in fluorescence at ~656 nm and 640 nm of more than 100 folds in vitro. At a concentration of 10 M, FS-ROS1 labels the L929 cell and Raw264.7 cell wells in 30 min with excellent biocompatibility and without washing. After labelling, FS-ROS1 exhibited a rational fluorescence increase upon the addition of 1, 10, 100 and 200 M of H2O2. Based on these results, inflammatory cells, stimulated with 800 nM dexamethasone and polyIC, showed a higher increase in fluorescence than the control cells. These results suggest that H2O2 and ClO- might be important signaling molecules during inflammations.